Lisinopril is an orally active angiotensin-converting enzyme (ACE) inhibitor which at dosages of 20 to 80mg once daily is effective in lowering blood pressure in all grades of essential hypertension. It is at least as effective as usual therapeutic dosages of hydro-chlorothiazide, atenolol, metoprolol and nifedipine while direct comparisons with other ACE inhibitors have not been reported. Many patients achieve an adequate blood pressure reduction with lisinopril alone, and in those who do not, most will with the addition of hydrochlorothiazide; lisinopril also attenuates hypokalaemia induced by thiazide diuretics. In patients with congestive heart failure resistant to conventional therapy, lisinopril 2.5 to 20mg once daily improved indices of cardiac function and appeared to produce greater benefit than captopril in one controlled study. Lisinopril is well tolerated, with few serious adverse effects being reported.
Thus, lisinopril is a suitable treatment for essential hypertension and shows promise in the treatment of congestive heart failure. If additional studies confirm these preliminary findings, then lisinopril will have a similar profile of indications to other ACE inhibitors, and like some other drugs in this class it offers the convenience of once daily administration.
Lisinopril is a lysine derivative of enalaprilat, the active angiotensin-converting enzyme (ACE) inhibitor metabolite of enalapril. Lisinopril decreases plasma concentrations of angiotensin II and aldosterone, and increases plasma renin activity. Most data support the hypothesis that the beneficial haemodynamic effects of lisinopril are caused by ACE inhibition and the consequent reduction in angiotensin II, which either directly or indirectly results in dilatation of peripheral vessels and reduced vascular resistance.
In healthy subjects single oral doses of lisinopril 10mg reduced blood pressure by approximately 15% after about 6 hours. In patients with mild to moderate essential hypertension the acute reduction in blood pressure was not increased with single oral doses greater than 5mg, although the duration of action was prolonged for more than 24 hours with doses up to 20mg. Vascular resistance is markedly reduced by lisinopril treatment in patients with hypertension or congestive heart failure, without significant changes in heart rate. The lack of reflex tachycardia does not appear to be related to a reduction in baroreceptor sensitivity.
In patients with severe congestive heart failure, acute administration of lisinopril 1.25 to 10mg reduces mean arterial pressure (about 15 to 20%) which is associated with beneficial cardiovascular changes [reduced systemic vascular resistance (about 25 to 35%), reduced pulmonary capillary wedge pressure (about 25 to 45%) and increased cardiac index (about 10 to 30%)]. Lisinopril treatment increases renal blood flow by about 16% in patients with essential hypertension, without affecting glomerular filtration rate.
About 25 to 50% of an oral dose of lisinopril is bioavailable in man and peak serum concentrations of lisinopril are reached in about 6 hours. Absorption is unaffected by food. Lisinopril is not significantly metabolised in humans and absorbed drug is primarily excreted unchanged in urine. Lisinopril has polyphasic elimination kinetics. Most of the drug is eliminated during the more rapid phase with an effective half-life of 12.6 hours. The terminal phase, with a half-life of 30 hours, represents saturable binding of lisinopril to plasma ACE. During once daily administration steady-state concentrations are achieved with 3 doses and accumulation is modest except in patients with severe renal impairment, and dosage reductions are necessary in such patients.
In non-comparative studies in patients with essential or renovascular hypertension lisinopril (up to 80mg once daily) produced reductions in systolic and diastolic blood pressures of about 15%. Furthermore, the duration of the antihypertensive effect of lisinopril in placebo-controlled studies was about 24 hours during once daily administration.
In mild to moderate essential hypertension lisinopril 20 to 80mg once daily was more effective than hydrochlorothiazide (up to 50 mg/day), and the combination of both these drugs produced even greater reductions in blood pressure than lisinopril alone. In addition, lisinopril may attenuate diuretic-induced reductions in serum potassium concentrations. Non-Black patients respond better to lisinopril, both alone and in combination with hydrochlorothiazide, than Black patients.
Lisinopril 20 to 80mg once daily appears to be at least as effective in lowering blood pressure as atenolol 50 to 200 mg/day or metoprolol 100 to 200 mg/day when used alone or in combination with hydrochlorothiazide in both young and elderly patients over 65 years of age. In addition, lisinopril has comparable antihypertensive efficacy to nifedipine 40 to 80 mg/day and is associated with a lower incidence of side effects and patient withdrawals.
Non-comparative studies and comparative trials with placebo and captopril in patients with severe congestive heart failure (CHF) maintained on digitalis and diuretics reported encouraging improvements in indices of cardiac function (increased cardiac index and ejection fraction, and decreased pulmonary capillary wedge pressure and systemic vascular resistance). Patients also show improvements in exercise performance, New York Heart Association Functional Class and associated symptomatology after receiving lisinopril (usually 5 to 20mg once daily) for up to 3 months. In one controlled study, lisinopril 5 to 20mg appeared to produce greater improvements in the signs and symptoms of CHF than captopril (up to 150 mg/day) in 129 patients. However, additional studies are needed to confirm this initial report.
The most frequently reported side effects during clinical trials with lisinopril included dizziness, headache, cough, hypotension and diarrhoea. The majority of these effects were mild, occurred with similar incidence rates in elderly and non-elderly (under 65 years) hypertensive patients and also occurred in some patients receiving placebo. Serious adverse effects with lisinopril were rare.
In comparison with captopril, in patients with congestive heart failure, lisinopril treatment produced a greater incidence of elevated blood urea nitrogen and plasma potassium concentrations, although these effects were clinically insignificant.
Dosage and Administration
The initial dosage in patients with normal renal function is 10mg once daily in hypertension and 2.5mg once daily in congestive heart failure. Doses can be increased according to patient response, up to a maximum of 20mg once daily in patients with congestive heart failure. The usual maintenance doses for the treatment of hypertension are in the range 20 to 40mg once daily. Most hypertensive patients not responding to lisinopril alone respond adequately to the addition of hydrochlorothiazide. In patients with congestive heart failure concomitant therapy with digitalis and/or diuretics should be continued. The initial dosage should be reduced to 2.5 to 5mg once daily in hypertensive patients with renal impairment or renal artery stenosis and may be titrated up to 40mg once daily according to patient response. Dose titration should be very gradual in patients with renal impairment and the possibility of symptomatic hypotension, in patients who are hypovolaemic due to diuretic therapy or salt restriction, can be minimised by discontinuation of the diuretic prior to the initiation of treatment with lisinopril.
In patients receiving potassium supplements or potassium-sparing diuretics lisinopril should be used with caution and with frequent monitoring of serum potassium concentrations.
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Various sections of the manuscript reviewed by: K. Arakawa, Department of Internal Medicine, University of Fukuoka, Fukuoka City, Japan; J. Biollaz, Department of Medicine, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland; A.M. Breckenridge, Department of Clinical Pharmacology, University of Liverpool, Liverpool, England; B.C. Campbell, University Department of Materia Medica, Stobhill General Hospital, Glasgow, Scotland; K. Dickstein, Cardiology Section, Central Hospital in Rogaland, Stavanger, Norway; J. Donohoe, Department of Nephrology, Mater Misericordiae Hospital, Dublin, Eire; A. Ebihara, Department of Clinical Pharmacology, Oita National Medical School, Oita-ken, Japan; G.P. Hodsman, Department of Medicine, University of Melbourne, Melbourne, Australia; D. Jewitt, Department of Cardiology, King’s College Hospital, London, England; B.E. Karlberg, Endocrine-Hypertension Unit, University Hospital, Linköping, Sweden; M.S. Kochar, Department of Medicine, The Medical College of Wisconsin, Milwaukee, Wisconsin, USA; K.R. Lees, University Department of Materia Medica, Stobhill General Hospital, Glasgow, Scotland; J.A. Millar, Department of Pharmacology, University of Otago, Dunedin, New Zealand; M. Moser, Davis Avenue Medical Center, White Plains, New York, USA; J.L. Reid, University Department of Materia Medica, Stobhill General Hospital, Glasgow, Scotland; P.J. Richardson, Department of Cardiology, King’s College Hospital, London, England; Y.K. Seedat, Department of Medicine, University of Natal, Durban, South Africa; J.D. Swales, Department of Medicine, Leicester Royal Infirmary, Leicester, England; G.S. Thind, Division of Cardiology, Department of Medicine, University of Louisville, Louisville, Kentucky, USA; P.H. Vlasses, Division of Clinical Pharmacology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania, USA; A. Zanchetti, Centro di Fisiologia Clinica e Ipertensione, Ospedale Maggiore di Milano, Milan, Italy.
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Lancaster, S.G., Todd, P.A. Lisinopril. Drugs 35, 646–669 (1988). https://doi.org/10.2165/00003495-198835060-00003
- Congestive Heart Failure